JSH-23（AbMole，M2786）是一种核因子κB（NF-κB）通路的抑制剂，IC50 为 7.1 μM，与BAY 11-7082类似，也通过靶向NF-κB p65亚基的核转位发挥调控作用。JSH-23可通过抑制NF-κB信号通路的激活，从而下调促炎因子（如IL-6、TNF-α）的表达。JSH-23在LPS（Lipopolysaccharides，脂多糖）诱导的脓毒症模型小鼠中，JSH-23（3 mg/kg）通过抑制NF-κB通路减轻了心脏损伤，并减少了M1型巨噬细胞极化[9]。JSH-23（CAS No.：749886-87-1）在SD大鼠骨质疏松模型中通过TRAF6/Rac1/NOX1通路抑制破骨细胞分化，同时增强成骨细胞的Nrf2/HO-1表达以维持骨稳态[10]。JSH-23也具有抗肿瘤活性，它可抑制MDA-MB-468三阴性乳腺癌细胞的增殖与迁移，并在HepG2肝癌细胞中通过诱导G2/M期阻滞抑制细胞生长。JSH-23在阿尔茨海默病相关研究中，可恢复Aβ肽注射后的大鼠海马CA1锥体神经元的电生理特性，逆转异常增强的Ih电流[11]。这些研究共同表明，JSH-23作为NF-κB通路的工具分子，在炎症调控、肿瘤干预、神经保护及骨代谢研究中具有重要价值。

QNZ（EVP4593，AbMole，M2298）是一种NF-κB抑制剂，可抑制 NF-κB 的转录调节活性（IC50为11 nM），QNZ通过靶向抑制p65蛋白（RelA亚基）发挥调控作用。EVP4593可在大鼠肺组织中抑制TLR4/MyD88/NF-κB信号通路，进而调控肺部的炎症反应。此外，EVP4593还是一种能够抑制Orai（钙释放激活钙通道）和TRPC（经典瞬时受体电位离子通道）的化合物，同时对SOCs（内源性储存操作钙通道）也表现出抑制作用[13]。QNZ（CAS No.：545380-34-5）不仅通过调节上述离子通道在亨廷顿病（HD）研究中有效降低突变型亨廷顿蛋白水平，还在诱导多能干细胞（iPSCs）分化的神经元模型中表现出神经保护作用[14]。

Andrographolide（ANDRO，穿心莲内酯，AbMole，M6444）是一种从植物穿心莲（Andrographis paniculata）中分离的二萜内酯化合物，具有抗炎、抗肿瘤、抗氧化等多种生物活性。Andrographolide（Andrographis）还是一种NF-κB信号通路的抑制剂，可通过共价修饰p50 的半胱氨酸残基，抑制NF-κB的激活。Andrographolide（CAS No.：5508-58-7）在Toll样受体（TLR）信号通路中，抑制TLR3和TLR4诱导的NF-κB活化，能显著降低COX-2等促炎因子的表达[16]。另外，Andrographolide还能直接干扰NF-κB与DNA启动子区域的结合，从而阻断下游促炎基因的转录[17]。

Dehydroxymethylepoxyquinomicin (DHMEQ，AbMole，M11454）是一种基于微生物次级代谢产物Eepoxyquinomicin C的结构设计合成的特异性NF-κB抑制剂[18]。DHMEQ（CAS No.：287194-40-5）主要通过环氧基团与NF-κB组分中特定半胱氨酸残基的SH基团结合，从而阻断NF-κB的DNA结合能力，抑制其转录活性[18]。DHMEQ作为特异性的NF-κB抑制剂，在探究NF-κB与炎症/肿瘤的相关信号网络方面具有重要价值[19]。例如DHMEQ可增加前列腺癌细胞对放疗的敏感性[20]，以及在胰岛组织的小鼠移植模型中降低组织损伤[21]。

IMD-0354（AbMole，M2769）是一种小分子IKKβ抑制剂，通过选择性阻断IKKβ活性，有效抑制经典NF-κB信号通路的激活[22]。IMD-0354（IKK2 Inhibitor V）的应用广泛，覆盖炎症、肿瘤及代谢研究。在细胞模型中，IMD-0354能有效抑制多种肿瘤细胞（如肺癌细胞、黑色素瘤细胞）的增殖，并通过阻断NF-κB依赖的MET激活，增强细胞对凋亡的敏感性[23]。IMD-0354还在小鼠过敏性炎症模型表现出抗过敏和抗炎效果，其核心机制同样依赖于对NF-κB通路的抑制[24]。

Caffeic Acid Phenethyl Ester（CAPE，咖啡酸苯乙酯，AbMole，M2484）是一种从蜂胶中提取的生物活性多酚酯，具有广泛的科研应用价值。其作用机理主要涉及抗氧化、抗炎、抑制NF-κB信号通路等。CAPE可在微摩尔浓度下抑制NF-κB通路，降低炎症因子的表达，因此具有强大的抗炎活性。例如Caffeic Acid Phenethyl Ester（CAS No.：104594-70-9）在胶原抗体诱导的关节炎小鼠中以 1 mg/kg的剂量，能显著减轻关节炎症和骨破坏[25]。类似地，CAPE 在牙周炎大鼠模型中以10 μmol/kg/天的剂量腹腔注射 14 天，能降低血清炎症因子（IL-1β、TNF-α）的水平[26]。Caffeic Acid Phenethyl Ester还具有抗菌和抗肿瘤活性，例如有文献使用CAPE 并在1 nM至10 μM 浓度范围内测试其细胞活性，其中 10 μM的浓度显著抑制了骨肉瘤细胞增殖[27]。CAPE7（咖啡酸苯乙酯）对植物乳杆菌的最小抑菌浓度（MIC）为 125 μg/mL[28]。

Bay 11-7085（AbMole，M2435）是一种特异性核因子κB（NF-κB）抑制剂，通过靶向NF-κB信号通路发挥作用。Bay 11-7083（CAS No.：196309-76-9）可抑制IκBα磷酸化，阻断p65核转位，从而下调NF-κB的转录活性[29]。研究表明，Bay 11-7085不仅能直接抑制NF-κB，还能通过诱导PTEN表达间接降低AKT磷酸化[29]。在多种细胞模型中，如人骨肉瘤细胞（143B、MG63）、胃癌细胞（HGC27、MKN45）和神经胶质瘤细胞（U251），Bay 11-7085（BAY 11-7083）以剂量依赖性方式显著抑制细胞增殖、迁移和侵袭能力，同时促进凋亡[30, 31]。例如，在HGC27细胞中，其24小时半数抑制浓度（IC50）为24.88 nM[30]。此外，该化合物还能下调炎症相关蛋白（如NLRP3、IL-1β、IL-18）和上调凋亡标志物（如caspase 3、Bax）的表达[31]。

SN50（AbMole，M10545）是一种特异性抑制核因子κB（NF-κB）信号通路的肽类抑制剂，其核心作用机制是通过阻断NF-κB p65亚基的核转位，从而抑制下游炎症相关基因的激活[32]。也有研究表明，SN50能显著减少NF-κB p65在细胞核内的积累，同时降低胞质和核提取物中p65蛋白水平[33]。SN50（CAS No.：213546-53-3）同样具有抗炎能力，例如可有效抑制 LPS（Lipopolysaccharides，脂多糖）诱导的小鼠肺损伤[34]。在大鼠模型中，SN50通过抑制NF-κB核转位，能减轻机械牵拉诱导的炎症反应，并降低内乳动脉中IL-6的生成[35]。

SC75741（AbMole，M4940）是一种特异性核因子κB（NF-κB）信号通路抑制剂，在多种细胞和动物模型中展现出广泛的科研应用价值。其作用机制主要通过直接抑制NF-κB的激活，从而调控下游炎症、免疫及细胞稳态相关通路。SC75741可以通过激活先天免疫，应对病毒复制和传播[36]，例如保护小鼠（注射剂量为5 mg/kg/天）免受禽流感病毒的感染[37]。SC75741也具有抗肿瘤活性，可协同RIP2抑制GSK583 抑制肿瘤干细胞[38]。

PDTC（吡咯烷二硫代氨基甲酸铵，AbMole，M4005）是一种特异性核因子κB（NF-κB）信号通路抑制剂，通过阻断IκB-α磷酸化和NF-κB p65核转位发挥功能。其生物学活性主要是抑制炎症因子（如TNF-α、IL-6、IL-1β）的表达。在细胞实验中，PDTC表现出多方面的调控作用。在GES-1胃黏膜细胞中，PDTC（2.5-60 μmol/L）可剂量依赖性地抑制壬基酚诱导的NF-κB/NLRP3通路激活，降低炎症因子释放[40]。Pyrrolidinedithiocarbamate ammonium（CAS No.：5108-96-3）在甲状腺癌细胞（BCPAP和PTC3-5）中，能抑制NF-κB蛋白表达，影响细胞增殖和迁移[41]。在动物模型中，PDTC（Ammonium pyrrolidinedithiocarbamate）对多种疾病模型具有改善作用：例如在DSS（Dextran sulfate sodium salt，葡聚糖硫酸钠，AbMole，M9443）诱导的溃疡性结肠炎小鼠中，PDTC通过抑制NF-κB活化，减少Th17细胞比例，降低促炎介质产生[42]。在慢性萎缩性胃炎（CAG）小鼠模型中，PDTC（100-200 mg/kg/day，灌胃8周）可减轻胃黏膜损伤[43]。

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